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1 in the presence of NADPH by cell-free assay (cytochrome c).
2 itin, eglin c, ribonuclease A, lysozyme, and cytochrome c).
3 a number of heme protein systems, including cytochromes c'.
6 with decreasing protein molecular mass: for cytochrome c (12.3 kDa) and lysozyme (14.3 kDa) a detect
7 (PNA) can be used to control the assembly of cytochrome c (12.5 kDa, pI 10.5) and azurin (13.9 kDa, p
8 exhibited significant rates of reduction of cytochrome c (160 min(-1), largely superoxide dismutase-
9 efficiently as wild type MSR but the rate of cytochrome c, 2,6-dichloroindophenol, and menadione redu
11 isotopes at the fundamental distribution of cytochrome c(+8) (m/z approximately 1549) were nearly ba
12 by DESI-MS, were 100% for melittin, 100% for cytochrome c, 90% for myoglobin, and 65% for bovine seru
13 properties are reminiscent of the A-state of cytochrome c, a compact denatured form found under acidi
14 fic ablation of the proapoptotic function of cytochrome c, a key regulator of mitochondria-mediated a
17 lso propose an orientation of membrane-bound cytochrome c, a protein for which the membrane orientati
19 om proteins; a deamidated tryptic peptide of cytochrome c, a tryptic peptide from unfolded and deamid
20 mitochondrial membrane potential, release of cytochrome c, activation of Bax and Bak, and processing
21 grity of mitochondria, leading to release of cytochrome c, activation of caspase-3 and eventually exe
22 Ad-MMP-9 infection induced the release of cytochrome c, activation of caspase-9 and -3, and cleava
23 mitochondrial permeability shift, release of cytochrome c, activation of caspases, and subsequent fra
24 res contained four basic proteins (lysozyme, cytochrome c, alpha-chymotrypsinogen A, and ribonuclease
27 (flavoprotein, succinate dehydrogenase, and cytochrome c) and the synthesis and activity of key deni
28 depolarizes mitochondria membranes, releases cytochrome c, and activates caspases-9 and -3 and death
29 hondrial membrane depolarization, release of cytochrome c, and activation of both intrinsic and extri
31 tial within 30 min, release of mitochondrial cytochrome c, and activation of caspase-activated DNase
32 chondrial proteins, release of the apoptogen cytochrome c, and activation of executioner caspase-3 we
33 islets was strongly correlated with reduced cytochrome c, and agents that acutely and specifically r
34 he release of Smac, Omi, adenylate kinase-2, cytochrome c, and apoptosis-inducing factor (AIF) during
35 ized HAzPC associated with mitochondria, and cytochrome c, and apoptosis-inducing factor escaped from
39 formed in ESI for three proteins (ubiquitin, cytochrome c, and carbonic anhydrase II) were investigat
41 Bax expression, a disturbed distribution of cytochrome c, and cleaved caspase-3 positive staining in
42 e purification of the engineered peroxidase, cytochrome c, and covalent complex, along with activity
44 aspase-8, deficient release of mitochondrial cytochrome c, and delayed activation of both caspase-9 a
45 duced unfolding of SNase, from acid-unfolded cytochrome c, and from folding of Azoarcus ribozyme.
46 in blocking apoptosis by reduction of ferric cytochrome c, and gentle tuning of NO concentration in t
48 enzymatic activity and immunoreactivity for cytochrome c, and identical functional properties shared
49 ious Mossbauer investigations on a bacterial cytochrome c, and is not reproduced by the simulations.
50 of the mass spectral response for myoglobin, cytochrome c, and lysozyme is presented for laser electr
53 as well as mitochondrial release of AIF and cytochrome c, and subsequent activation of caspase-9 in
54 on of the effector caspase-9, independent of cytochrome c, and subsequently the processing of the exe
55 mitochondrial truncated Bid, the release of cytochrome c, and the activation of caspase-3, thereby c
56 f caspases, apoptogenic mitochondrial factor cytochrome c, and the Bcl-2 family proteins in DR6-induc
57 R) in portal blood, the release of cytosolic cytochrome c, and the cleaved caspase 9 expression in in
58 cular, appeared to be restricted to nitrated cytochrome c, and thus, no association of non-nitrated c
59 elease, lipid peroxidation, translocation of cytochrome c, and TUNEL labeling in the ischemic cortex.
61 esults constitute the molecular mechanism of cytochrome c- and dATP-mediated activation of Apaf-1.
62 2 positions (C(18:2)/C(18:2)), formed in the cytochrome c- and H(2)O(2)-driven enzymatic oxidation re
63 acid-binding protein, myoglobin and somatic cytochrome-C) and others (creatine kinase M, malate dehy
64 e myocardial levels of lipid hydroperoxides, cytochrome-c, and mitochondrial aconitase activity were
65 ns c-Jun N-terminal kinase 3, caspase 3, and cytochrome C, Annexin V staining, RNA degradation, and o
66 tryptophans in three well-studied proteins, cytochrome c, apomyoglobin, and lysozyme, as a function
67 her a caspase-dependent mechanism, involving cytochrome c, apoptosis protease-activating factor-1 (Ap
68 avage; and Bcl-2 phosphorylation, as well as cytochrome c, apoptosis-inducing factor (AIF), and endon
70 D ( approximately 16% decrease, males only), cytochrome C ( approximately 19% decrease, females only)
71 ase of intermembrane space proteins, such as cytochrome c, are early events during intrinsic (mitocho
74 a picosecond timescale for the heme protein, cytochrome c, as a function of oxidation and hydration,
75 gment-elevation AMI patients with detectable cytochrome c, as compared with those with nondetectable
76 s approach to the absolute quantification of cytochrome C (as target compound) in a commercial protei
77 terial heme protein Alcaligenes xylosoxidans cytochrome c' (AXCP) forms a novel five-coordinate heme-
79 % (w/v) bovine serum albumin and 0.01% (w/v) cytochrome C (both are proteins), and 0.002% (w/v) human
80 ation and identification of proteins such as cytochrome c, bovine serum albumin, and high-molecular w
81 brane pores large enough to release not only cytochrome c, but also allophycocyanine, a protein of 10
82 erobic electron acceptors include oxygen and cytochrome c, but an acceptor that can function under an
83 electrons coming from NADH and ubiquinol to cytochrome c, but it is also capable of producing signif
84 sequent release of the mitochondrial protein cytochrome c, but the second mitochondrion-derived activ
86 a result, during steady-state turnover with cytochrome c, calmodulin now deactivates the enzyme and
87 induced mitochondrial trafficking of Bax and cytochrome c, caspase-3 activation, and oxidative stress
88 he product of the enzymatic reaction reduces cytochrome c, causing an increase in absorbance at 550 n
92 s to the periplasmic enzymes that reduce apo-cytochrome c (CcsX) or repair oxidative protein damages
93 H2O2-dependent apoptosis in mouse embryonic cytochrome c(+/+) cells than in cytochrome c(-/-) cells.
96 ria differed primarily at a Raman biomarker, cytochrome c, corresponding to a bacteroid-specific term
97 arkers of WAT mitochondrial protein content (cytochrome c, COXIV-subunit I, and citrate synthase acti
100 and the nuclear-encoded subunits of COX and cytochrome c (CYC), we hypothesized that some codons in
101 lus fumigatus alternative oxidase (aoxA) and cytochrome C (cycA) null mutants and assessed their abil
102 rving as respiratory electron shuttle, ferri-cytochrome c (cyt c) acts as a peroxidase; i.e., it cata
103 ns and ER stress as shown by increased HSP60/Cytochrome C (Cyt C) and CHOP-ATF3 levels respectively.
104 d, catalytic circuit based on photosystem I, cytochrome c (cyt c) and human sulfite oxidase (hSOX).
105 An axial S(Met) bond is also present in cytochrome c (cyt c) and is generally thought to increas
106 tive stress sensor contains the heme protein cytochrome c (cyt c) as sensing element whose spectral r
108 tivation of peroxidase catalytic function of cytochrome c (cyt c) by anionic lipids is associated wit
109 y to investigate the early folding states of Cytochrome c (cyt c) by monitoring the distance between
110 ted for the first time that the heme protein cytochrome c (Cyt c) can enter the interior of a MOF des
112 cribe advancements in sensing technology for cytochrome c (cyt c) detection, at point-of-care (POC) a
116 denatured states and the native structure of cytochrome c (Cyt c) from Saccharomyces cerevisiae.
117 activation is accompanied by the release of cytochrome c (cyt c) from the intermembrane gap and subs
122 competent peroxidase form of pentacoordinate cytochrome c (cyt c) in a complex with a mitochondria-sp
123 vine serum albumin (BSA), lysozyme (lyz) and cytochrome c (cyt c) in singular and competitive manner
124 of Thr78Cys/Lys79Gly/Met80X mutants of yeast cytochrome c (cyt c) in which Cys78 becomes one of the a
134 arly mitochondria-specific cardiolipin (CL), cytochrome c (cyt c) loses its tertiary structure and it
135 cytochrome c synthase (HCCS) is required for cytochrome c (cyt c) maturation and therefore respiratio
138 tion of cardiolipin (CL) by its complex with cytochrome c (cyt c) plays a crucial role in triggering
140 has been suggested that the alkaline form of cytochrome c (cyt c) regulates function of this protein
141 tic stress induces apoptosis, which involves cytochrome c (Cyt c) release from mitochondria and subse
144 s of the spontaneous reversible unfolding of Cytochrome c (Cyt c) under native conditions have led to
150 interaction of the simple, globular protein cytochrome C (Cyt C) with MPMN surfaces using experiment
151 rochemical immunosensor for the detection of cytochrome c (cyt c), a heme containing metalloprotein u
156 nsfer reorganization free energy (lambda) of cytochrome c (Cyt) in electrostatic complexes that mimic
160 hieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized
163 as an oligopeptide stopper, we have employed cytochrome C (CytC) as a protein stopper to produce the
167 r the directed immobilization of horse heart cytochrome c (cytc) on gold electrode surfaces to achiev
168 tion (MOMP) via BAK and BAX oligomerization, cytochrome c (cytc) release, and caspase activation are
170 -phycoerythrin (R-PE) and positively charged cytochrome c (CYTC) within the same DFGF apparatus is sh
171 te ETp across the electron-mediating protein cytochrome c (CytC), measured in a monolayer configurati
174 rate synthase), and the expression levels of cytochrome c, cytochrome c oxidase subunit 1, and mitoch
175 + H2O) with electrons donated by periplasmic cytochrome c (cytochrome c-dependent NO reductase; cNOR)
176 hibitor, prevented the increase in cytosolic cytochrome c, decreased caspase-3 activation, and partia
177 , exercise-induced increases in the mRNAs of cytochrome c, delta-aminolevulinate synthase, and citrat
178 polarization of mitochondria, and release of cytochrome c, demonstrating its important role as an ant
180 es for all three monomeric proteins, and for cytochrome c, dimers of significant intensity are also o
181 in an observed sequence coverage of 79% for cytochrome C (eight peptides), 47% for beta-lactoglobuli
182 hampers mitochondrial respiration, releases cytochrome c, elevates mitochondrial lipid peroxidation,
183 ectron transfer-triggered folding of reduced cytochrome c, far-UV time-resolved circular dichroism (T
184 65 mM SDS to induce the MG state in oxidized cytochrome c, folding of redcyt c was triggered with fas
186 -coordinate heme-nitrosyl complex (5c-NO) of cytochrome c' from Alcaligenes xylosoxidans (AXCP) in wh
187 either heme face exists, as in the microbial cytochrome c' from Alcaligenes xylosoxidans (AxCYTcp), w
191 re reveals a core that is typical of class I cytochromes c, having alpha-helices folded into a compac
193 -Volmer quenching constants (Ksv) for hemin, cytochrome c, hemoglobin, and myoglobin were 5.6x10(7),
194 ta defensin 1, truncated human lymphotactin, Cytochrome C, holo hemoglobin-alpha, ovalbumin, human tr
195 ged: the first was to maintain the KD of the cytochrome c' in the 1 microM range, and the second was
197 n conformations of a small globular protein, cytochrome c, in the presence of guanidine hydrochloride
198 d had greater amounts of cytosolic mtDNA and cytochrome c, increased apoptosis, and more IL-1beta sec
199 eased activation of caspase-3 and release of cytochrome c, indicating that a mitochondrial pathway wa
200 lding proteins, including alpha-lactalbumin, cytochrome c, intestinal fatty acid binding protein (IFA
202 wnstream of the mitochondria, with cytosolic cytochrome c, kills brain tumor cells but not normal bra
203 nents abolishes the ability of cells to form cytochrome c, leading in the case of Rhodobacter capsula
205 mP in a complex with its substrate, L. major cytochrome c (LmCytc) to 1.84 A, and compared the struct
207 volves mitochondria, indicated by release of cytochrome c, loss of mitochondrial membrane potential a
209 ion to peptides, gas-phase HDX of ubiquitin, cytochrome c, lysozyme, and apomyoglobin were examined.
213 (NANOG, MYOD), antibodies, native proteins (cytochrome C), magnetic nanoparticles (MNPs), and nuclei
215 horylation and fatty acid oxidation, such as cytochrome c, medium-chain acyl-CoA dehydrogenase, and a
217 dione or benzoquinone and weak activity with cytochrome c, molecular oxygen, and 5,5'-dithio-bis-2-ni
218 releases of a small protein (8 muL of 5 muM cytochrome-c, molecular mass ~12 kDa) and exhibits ~1 mi
222 A mixture containing four model proteins (cytochrome c, myoglobin, bovine serum albumin (BSA), and
223 the transport of electrons from ubiquinol to cytochrome c (or alternate physiological acceptors), yet
224 V(max) of each in four assays: reduction of cytochrome c, oxidation of NADPH, 17alpha-hydroxylase ac
227 tra of the B-bands of bovine and horse heart cytochrome c (pH 7.0) exhibit a pronounced couplet that
228 tensity caused by the alkaline transition of cytochrome c (pH 7.0-9.5), and (ii) an increase in inten
229 , Apaf-1, procaspase-9, procaspase-3, Hsp70, cytochrome c, PHAPI, CAS, and regulatory compounds to mi
230 -to-Bcl-2 ratio (R(2) = 0.83) and release of cytochrome c (R(2) = 0.92), but preceded in time the cas
232 old on a sub-millisecond time scale, whereas cytochrome c' refolding requires 10 s or more to complet
234 d to be 350 and 25 mg/ml for rusticyanin and cytochrome c, respectively; cytochrome a was present as
237 the refolding of Rhodopseudomonas palustris cytochrome c' reveals dramatic differences between two v
238 -based apoptotic pathway involved release of cytochrome c, second mitochondria-derived activator of c
240 -cytochrome c and Rhodopseudomonas palustris cytochrome c', shows that foldable sequences deviate sig
241 anied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase
245 pathological changes and increased levels of cytochrome c, Smac/DIABLO and AIF in the cytosol while t
246 ay, leading to increased cytosolic levels of cytochrome c, Smac/Diablo and Omi/HtrA2, and activation
247 embrane potential, attenuated the release of cytochrome c, Smac/DIABLO, and apoptosis inducing factor
248 mitochondrial depolarization and release of cytochrome c, Smac/DIABLO, and apoptosis-inducing factor
249 e swelling was accompanied by the release of cytochrome c, Smac/DIABLO, Omi/HtrA2, and AIF but not en
250 The protein expressions of mitochondrial cytochrome c, stromal cell-derived factor-1, C-X-C chemo
251 ebrovascular mitochondria, such as ER-alpha, cytochrome c, subunit IV of complex IV, and manganese su
252 n transferase activity with equine and yeast cytochrome c, suggesting a conservation of the enzymatic
253 Apaf-1 and rendered the cells insensitive to cytochrome c, suggesting a potential role for Rsk signal
254 th released the apoptogenic factors Smac and cytochrome c, suggesting that they are primed for cell d
255 o affect the buried hydrogen bond network of cytochrome c, suggesting that this network is an importa
256 While the N-terminal domain is a class I cytochrome c, the C-terminal domain shows no similarity
257 ee proteins of increasing intrinsic disorder-cytochrome c, the tumor suppressor protein p53 DNA bindi
258 The surprising finding is that, unlike for cytochrome c, there is an observable folding intermediat
260 imilar to the previously reported results on cytochrome c, these fragment ions form near residues kno
261 d in the presence of cytosol did not release cytochrome c, they displayed a dramatic increase in sens
262 that reduced DSD-Fdm transfers electrons to cytochrome c, thus generating the reduced cyt c stoichio
263 r binding affinity of rebaudioside A towards cytochrome c, thus supporting their host-guest relations
265 id hydrolysis to degrade a standard protein, cytochrome c, to produce many di/tripeptides with known
267 t with MPH (10mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10mg/kg) increas
268 abilities are demonstrated for ubiquitin and cytochrome c, two common model proteins for structure an
269 obilities of single multiply charged ions of cytochrome c, ubiquitin, myoglobin, and bovine serum alb
271 ein SERS spectra of a layer of test protein, Cytochrome-c, using a custom-made Otto-Raman spectroscop
272 reactivity of the reduced FMN domain toward cytochrome c; (v) response to calmodulin binding; and (v
273 y mixed-spin (sextet-quartet) heme center in cytochrome c' was investigated by electron nuclear doubl
275 of model proteins in aqueous media, such as cytochrome c, was also examined, yielding spectra with a
277 functionally relevant structural changes in cytochrome c, we measured the absorption and electronic
278 er metal porphyrins can be incorporated into cytochromes c, we engineered Escherichia coli so that th
279 ins (transferrin, myoglobin, hemoglobin, and cytochrome c) were separated by high-performance liquid
280 ng dichlorodihydrofluorescence diacetate and cytochrome c, were rapidly and significantly increased f
281 the SH3 domain, dihydrofolate reductase, and cytochrome c, where the transparent window vibrational p
282 calmodulin (CaM)-free and CaM-bound nNOS to cytochrome c, whereas hinge lengthening relieved repress
283 ngly abolish formation of both holo-CcmE and cytochrome c, whereas previously reported point mutation
284 MOM permeabilization, causing the release of cytochrome c, which effectively commits the cell to die.
286 eabilization (MOMP), allowing the release of cytochrome c, which interacts with Apaf-1 to trigger cas
287 Later, the cell body mitochondria release cytochrome c, which is followed by caspase activation, a
288 tion and inhibits the peroxidase activity of cytochrome c, which is involved in its release from mito
290 2)S also reduces CcO's biological reductant, cytochrome c, which normally derives its reducing equiva
291 hondrial damage and translocation of Bax and cytochrome c, which were then followed by caspase-3 acti
292 n aberrant activation of a testis isoform of cytochrome c, which, albeit expressed at low levels, was
293 different proteins (Trp-cage, myoglobin, and cytochrome c) with folding time constants that differ by
294 1 functioned as a translational repressor of cytochrome c, with interventions to silence TIA-1 dramat
295 erric forms of Met80X mutants of yeast iso-1-cytochrome c (X = Ala, Ser, Asp, and Glu) display EPR an
296 roxidase (ZnCcP) in complex with yeast iso-1-cytochrome c (yCc) diffract to higher resolution (1.7 A)
297 ection values of the charge states of equine cytochrome c (z = 9-16), and values are in good agreemen
298 e demonstrate that Zn(II) porphyrin in Zn(II)cytochrome c (Zn cyt c) is a fluorescence resonance ener
299 phyrin (ZnP) chromophore in zinc-substituted cytochrome c (Zn-cyt c) and an Alexa Fluor dye attached
300 ctron-transfer reactions of zinc-substituted cytochrome c, ZnCyt-c, immobilized on mesoporous, nanocr
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